11 Mitral valve disease Flashcards
In which views are which MV scallops visualised?
In the PLAX view, A2 and P2 are visualised.
In the PSAX view A3-A1 and P3-P1 are visualised.
In the A4C view, A2/A3 and P1 are visualised.
In the A2C view, P3, A2 and P1 are visualised.
In the A3C view, A2 and P2 are visualised.
Describe the M-mode of the MV in the PLAX view.
The MV opens in early diastole when the blood passively flows from the LA into the LV. The E point is the most anterior point of the anterior MV leaflet. The tips move towards the other during mid diastole and move away from the other during end diastole when blood actively flows from the LA to the LV. The A point is the point of the anterior MV leaflet during this phase. The MV closes at the start of systole.
What are the causes of MS?
Calcification, RHD, IE, congenital, LA masses and cor triatriatum.
In calcific MS, mitral annular calcification can spread to the mitral leaflets to cause MS.
In rheumatic MS, bacterial infection causes inflammation. This causes fibrosis and scarring, and, therefore, thickening, calcification, and commissural fusion, of the MV. Rheumatic MS also causes chordal fibrosis, thickening and shortening. This restricts MV mobility.
In IE, the bacterial infection causes vegetations on the MV which damage the leaflets.
The congenital causes of MS include congenital MS (MV dysplasia or hypoplasia), parachute MV (the chordae tendineae are attached to one papillary muscle, not two), subvalvular MV ring (a fibrous/muscular ridge in the LA which obstructs blood flow), double orifice MV (the two orifices decrease the MV orifice area), and Shone’s complex (parachute MV and supravalvular MV ring).
LA myxomas and tumours can obstruct the MV during diastole and intermittently block the MV opening, via prolapse into the MV opening, causing functional MS. Myxomas and tumours can damage the MV.
Cor-triatriatum is a congenital heart disease in which the LA is divided into two chambers by a fibromuscular membrane. The MV is anatomically normal but the membrane causes obstruction and functional MS.
What are the TTE characteristics of MS?
Thickened and calcified MV leaflets, restricted MV leaflets, decreased MVA, increased MV Vmax, and/or increased MV PG.
In calcific MS, there is mitral annular calcification.
In rheumatic MS, there are hockey stick shaped leaflets with thin stalks and thick tips, free leaflet edges with commissural fusion and leaflet diastolic doming.
In IE, there are vegetations.
LA mass with dynamic MV obstruction.
In cor triatriatum there is a LA fibromuscular membrane.
What are the symptoms and signs of MS?
Dyspnoea, cough, haemoptysis (pulmonary hypertension causes pulmonary vasculature rupture), peripheral oedema and/or emboli.
AF, malar flush, tapping apex beat, loud S1, loud P2 to S2, P2 in the presence of pulmonary hypertension, opening snap and/or low pitched mid diastolic murmur with presystolic exacerbation.
What are the quantitative methods used to assess MS?
MVA (planimetry or the continuity equation), mean PG and PHT.
How is MVA calculated in MS?
MVA is measured using planimetry by tracing the MV during diastole in the PSAX view.
MVA is calculated using the continuity equation.
CSA LVOT = 0.785 x (LVOT diameter)2
SV LVOT = CSA LVOT x VTI LVOT
SV MV = SV LVOT
MVA = SV MV / VTI MV
MVA = (LVOT CSA x LVOT VTI) / MV VTI
MVA is estimated using PHT.
MVA = 220 / PHT
The estimated MVA (PHT) is independent of MR but is dependent on factors affecting LA and/or LV compliance (ASDs and AR).
How is PHT affected by MS?
In severe MS, the PHT is longer. This is because the transmitral PG is higher so it takes longer for the pressure to decrease.
What is the Wilkin’s score?
The Wilkins score assesses MS severity and predicts the probability of MV balloon valvuloplasty success. A Wilkins score of >8 indicates a low probability of success. The Wilkins score is based on leaflet mobility, valvular thickening, subvalvular thickening and valvular calcification.
Leaflet mobility (mobile = 1; immobile = 4). Valvular thickening (normal (<5mm) = 1; severe thickening (8–10 mm) = 4). Subvalvular thickening (normal thickening = 1; global thickening = 4). Valvular calcification (low echogenicity = 1; high echogenicity = 4).
What are the effects of MS on chamber size and function?
Normal LV size with normal systolic function, LV diastolic dysfunction, LA dilatation, decreased LA strain, pulmonary hypertension and pulmonary congestion, RV hypertrophy, dilatation and dysfunction (chronically).
MS causes LA pressure overload which causes LA dilatation. This decreases LA strain and increases the risk of AF. This causes pulmonary hypertension and the symptoms of pulmonary congestion. Chronically, this also causes RV hypertrophy, dilatation and dysfunction, causing right sided HF and TR.
How is MS assessed using exercise stress echo?
In patients with MS with symptoms which are not proportional to the echo measurements, exercise stress echo is performed to identify patients who would benefit from treatment. Treatment is indicated in patients with exertional dyspnoea with a mean transmitral PG of >15mmHg and PASP of >60mmHg.
What are the BSE values for the assessment of MS?
…
What are the causes of primary MR?
Prolapse, RHD, IE, mitral annular calcification, drug/radiation induced and congenital.
Myxomatous MV degeneration causes uni-leaflet or bi-leaflet prolapse of the MV into the LA during systole. The myxomatous degeneration causes leaflet thickening and elongation and chordae elongation and rupture. This causes prolapse which impairs coaptation.
In rheumatic MR, bacterial infection causes inflammation. This causes fibrosis and scarring, and, therefore, thickening, calcification, and commissural fusion, of the MV. Rheumatic MS also causes chordal fibrosis, thickening and shortening. This impairs MV coaptation.
In IE, the bacterial infection causes vegetations on the MV which damage the leaflets.
In mitral annular calcification, calcium builds up on the annulus which increases the stiffness and decreases the mobility of the mitral annulus. This deforms the mitral annulus which impairs leaflet coaptation. Annular calcification can cause leaflet calcification which can further impair leaflet coaptation.
Serotonergic drugs can increase leaflet thickness and decrease leaflet mobility, causing primary MR, and chemotherapeutic drugs can cause LV impairment, causing secondary MR. Radiation can increase leaflet thickness and decrease leaflet mobility via inflammation, increase annular calcification and stiffness which decreases leaflet coaptation, and cause LV impairment causing secondary MR.
The congenital causes of MS include congenital MS (MV dysplasia or hypoplasia), parachute MV (the chordae tendineae are attached to one papillary muscle, not two), subvalvular MV ring (a fibrous/muscular ridge in the LA which obstructs blood flow), double orifice MV (the two orifices decrease the MV orifice area), and Shone’s complex (parachute MV and supravalvular MV ring).
What are the TTE characteristics of primary MR?
Thickened MV leaflets, impaired MV coaptation and systolic regurgitant flow.
In MVP, there is leaflet displacement of >2mm below the level of the annulus during systole. Leaflet billowing/prolapse/flail, elongated leaflets, thickened leaflets, excessive leaflet movement during systole, elongated chordae, annular dilatation and/or posteriorly directed MR.
In rheumatic MR, there are hockey stick shaped leaflets with thin stalks and thick tips, free leaflet edges with commissural fusion and leaflet diastolic doming.
In IE, there are vegetations.
What are the causes of secondary MR?
Infarction and acute papillary muscle rupture. Ischemia and chronic LV changes.
In MR secondary to infarction, papillary muscle rupture causes leaflet flail. Normally, the papillary muscle, with its chordae tendineae attached, prolapses into the LA during systole. This causes acute severe eccentric MR.
In symmetric ischemic MR, global LV dilatation causes bi-papillary muscle displacement and mitral annular dilatation which impairs leaflet coaptation. This causes central MR. In asymmetric MR, abnormal posterior (inferolateral) LV wall motion posteromedial papillary muscle displacement which causes posterior leaflet displacement and secondary chordae (anterior leaflet) tethering. This causes eccentric posteriorly directed MR.
What are the TTE characteristics of secondary MR?
LV systolic dysfunction with RWMAs, papillary muscle displacement and/or impaired MV coaptation with eccentric MR jet.
LV dilatation, papillary muscle displacement, mitral annular dilatation, MV leaflet tethering and/or central or eccentric MR.
What are the symptoms and signs of MR?
HF symptoms and symptoms of the underlying cause.
AF, displaced apex beat (LV dilatation), pansystolic murmur (apex), mid to late systolic click with late systolic murmur (MVP) and/or HF signs (severe chronic MR or acute MR).
What are the effects of MR on chamber size and function?
Acute MR increases LA pressure but not LA size and increases LV (end diastolic) pressure causing LV systolic dysfunction (acute HF) but not LV dilatation. Acute MR causes severe pulmonary hypertension, which suddenly increases the PASP, causing RV dysfunction (acute HF) but not RV dilatation.
Chronic MR increases LA pressure causing LA dilatation and increases LV (end diastolic) pressure causing eccentric hypertrophy and dilatation causing LV systolic dysfunction. Chronic MR causes mild pulmonary hypertension, which slowly increases the PASP, causing RV dilatation and RV dysfunction which causes TR.
How are acute and chronic MR differentiated?
In acute MR the LA volume and LA pressure increase suddenly and pulmonary vein pressure increases causing acute pulmonary oedema. However, the LA size and LV size and function are normal. Patients present with new onset dyspnoea and PND. Pulmonary hypertension is acute and severe. Acute MR may be due to chordae tendineae rupture, papillary muscle rupture or IE. Differential diagnoses include acute HF, PE and/or aortic dissection.
In chronic MR, the LA volume and LA pressure increase slowly. The LA dilates to compensate for the increased LA volume and the LV eccentrically hypertrophies and dilates to compensate for the increased preload and to maintain CO. Patients present with progressive dyspnoea and PND, AF and palpitations, and peripheral oedema. Pulmonary hypertension is slow and mild. Chronic MR may be due to MVP, RHD, or cardiomyopathies. Differential diagnoses include cardiomyopathies, AV disease, and primary pulmonary hypertension.
The MR velocity is high (e.g. 5m/s). In acute MR, the CWD velocity decreases throughout systole because the transmitral PG equalises faster than in chronic MR because the LA is not dilated. In chronic MR, the CWD is high throughout systole because the LA is dilated.
What is the Carpentier classification?
The Carpentier classification system is used to classify MR severity based on leaflet motion.
Type 1 is normal leaflet motion in which the MR is due to annular dilatation or leaflet perforation.
Type 2 is excessive leaflet motion in which the MR is due to leaflet prolapse or flail secondary to chordal elongation or rupture.
Type 3 is restricted leaflet motion in which the MR is due to leaflet tethering or restricted leaflet motion during systole (Type IIIb) or both systole and diastole (Type IIIa).
What are the qualitative methods used to assess MR?
MR size (MR jet size to LA size), MR origin, and MR direction (central or eccentric).
LA dilatation, LV dilatation and dysfunction, pulmonary vein systolic flow reversal and pulmonary hypertension.
How are eccentric MR jets assessed?
Central MR jets appear more severe because of the entrainment (blood cells on the side of the MR jet are drawn with the MR jet). Eccentric jets appear less severe because of the absence of entrainment on the side of the MR jet against the LA wall.
Normally, eccentric MR jets are directed in the opposite direction to the abnormal mitral leaflet (e.g. anterior leaflet prolapse causes a posterior MR jet).
What are the quantitative methods used to assess MR?
Regurgitant area, regurgitant volume, regurgitant fraction, VC, PISA, SV, MV inflow VTI/LVOT VTI
What happens to the SV in MR?
Normally, the volume of blood entering the LV, via the MV, during diastole equals the volume of blood exiting the LV (SV), via the LVOT, during systole. In MR, the LVOT outflow is less than MV inflow. Regurgitant volume = MV inflow volume – LVOT outflow volume.
